What causes stuttering? -> According to Ambrose (PhD researcher)

What causes stuttering? -> According to Ambrose (PhD researcher) The curious PWS (person who stutters) in me read [this](https://pubs.asha.org/doi/epdf/10.1044/cicsd_31_S_80) research. After finishing the 12 pages, I summed up the key points. **Goal** * Presenting theories in psychology, learning theory, and biology **Intro** * Genetic, physiologic, psychologic, and environmental influences guide the developmental pathway of stuttering. * Demosthenes practiced fluency with the noise of the waves in his ears, and now the stimulus of the waves evokes a learned response resulting in fluent speech (skinner) * perhaps many beliefs come from the left brain trying to explain what the right brain is experiencing **Psychologic Causes** * Psychoanalytic viewpoint: Travis described stuttering as a vehicle that acts to inhibit unconscious needs, or unacceptable statements of true inner thoughts and feelings. The child wants to communicate, but, being afraid of revealing unspeakable thoughts and feelings, he emits stuttered speech that conceals them. Any discomfort caused by the stuttering was, allegedly, more than overcome by the relief of hiding unmentionables * Glauber: the preponderance of stuttering in males was explained in psychologic terms in that boys faced more pressure to live up to standards of aggression and had a greater ability to provide and take action. Females, so it was said, had only to be passive individuals (Schuell) * **People who stutter (PWS)** are not any more neurotic than average * The only areas identified as problematic involved communication situations, difficulties that can be explained as resulting from the stuttering rather than being a cause of it. * Craig (2003): trait anxiety doesn't change versus state anxiety that changes in each situation. **Adults who stutter (AWS)** did present higher trait anxiety levels, but the anxiety appeared to have developed as a result of the stuttering and so would not be considered a causal factor. * psychosocial aspects of stuttering with a focus on temperament: Anderson (2003) found that stuttering children were less adaptable to novel situations, less distractible, and less regular in daily physiologic functions * However, the point of interest to the discussion here lies in a chicken and egg question: Do the differing temperament dimensions precipitate or exacerbate stuttering, or does the stuttering reinforce the temperamental proclivities of the child? **Behaviorism and Learning Theory** * Is stuttering a learned behavior or a “bad habit”? * Wingate (1997) states that below theories are forces in stuttering development: * Wendell Johnson’s diagnosogenic theory states that stuttering begins in the ears of the parents when they overreact to their child’s normal disfluencies. The child attempts to avoid the disfluencies and, in the struggle, stuttering develops. * Wischner states that stuttering originates from a painful, anxiety-producing stimulation in the form of parental disapproval of normal disfluency. In other words, the child anticipates negative, painful reactions to his or her stuttering and so tries to avoid them. Initial successful avoidance reduces the anxiety drive and thus reinforces the behavior that eventually becomes more complicated stuttering. * Sheehan: Stuttering results from an approach–avoidance drive. The desire to communicate collides with the drive to avoid speech anxiety, which may have roots in either or both personality and conditioning from prior negative experiences with stuttering. * Bloodstein: Stuttering is an anticipatory struggle arising from the belief that speech is difficult. Stuttering is seen as a reflection of tension and fragmentation in speech when the complexity of the act causes concern and feelings of being overwhelmed. * Ambrose: Stuttering behavior is acquired through operant conditioning shaped by its own consequences. * Flanagan found that stuttering was reduced when stuttered events were immediately followed by punishment (loud noise); it was increased when stuttered events were immediately followed by the removal of punishment (continuous tone) * Shames & Sherrick state that stuttering is shaped out of normal disfluency as operant behavior, subject to a combination of punishment, positive reinforcement, and negative reinforcement. Normal repetitions are reinforced when a parent eventually heeds the child’s request. But as repetitions become aversive, the parent indicates displeasure at disfluency (in terms of operant behavior, punishment). When the consequences of disfluency are negative reactions, the child may change disfluencies into struggle behavior or silence in order to avoid the aversive consequences (negative reinforcement for the parent). Thus, stuttering emerges by complex interaction of positive and negative reinforcement. * Brutten & Shoemaker's two-factor theory of stuttering: Stuttering is initially established through classical conditioning of emotional learning, when anxiety causes disruptions in speech. Through generalization, many stimuli acquire the capability of triggering anxiety that results in fluency breakdowns—stuttering. # Biologic Causes **Auditory feedback** * Ambrose: Stuttering reduces in noisy environments * Shane demonstrated that both stuttering and anxiety was reduced when PWS cannot hear themselves * Cherry and Sayers states that PWS have abnormal auditory feedback, and that the noise works because it neutralizes the defective auditory feedback. They concluded that stuttering is a perceptual problem. Yairi tends to agree * In normal speakers, the left planum temporale, part of the auditory association cortex, is larger in the left than the right hemisphere. In some individuals who stutter, however, this structural difference is reduced (Foundas, 2001). * Ingham (2000) found deactivation in auditory association cortex (in the temporal lobe, which includes Wernicke’s area), especially in the right-hemisphere, in adults who stutter as compared to normally fluent speakers. * Salmelin (1998) concluded that interhemispheric balance in the auditory cortex appears to be unstable in PWS **Central processing and sensorimotor integration** * **Language** * Involvement of language in stuttering: phonology, syntax, semantics, and cognitive processing. * There seems to be a higher incidence of the co-occurrence of stuttering and phonological disorders * Postma and Kolk's covert repair hypothesis: Stuttering is explained as self-repairs. Monitoring and error detection can occur at the prearticulatory level. Disfluencies are seen as by-products of covert repairs of internal speech errors, at the level of phonological encoding. When correction is successful, no error appears, but it may impede progress of an utterance, thereby leading to disfluency. PWS may have a deficit in phonological encoding, leading to more frequent phonological encoding errors, which must frequently be repaired, which leads to stuttering * **Linguistic complexity** * As mean length of unit (MLU) and syntactic complexity increase (Yaruss), and unfamiliar vocabulary (Hubbard), stuttering is more frequent * Ambrose: Phonological planning is aberrant in PWS * Ingham (2000) found clear differences in activation of the anterior insula in the frontal lobe, which is presumed to involve phonological planning. * **Sensorimotor integration** * Areas used for comprehension, planning, and production of speech show a high degree of connectivity in the left hemisphere for normal speakers. Sommer (2002) found that PWS showed significantly less fiber coherence, or myelin organization, in the area of the left rolandic operculum, which contains connections from the temporal to frontal lobes in areas subserving speech. The arcuate fasciculus (the bridge between Wernicke’s and Broca’s area), is included in this area. They concluded that overactivation of the right hemisphere in PWS may represent a compensatory strategy. * **Motor planning and execution** * Does the deficit underlying stuttering extend to more than speech? (e.g., performing more poorly across the motor systems as the task conditions become more difficult) * Zimmermann states: If the range is exceeded due to emotional, perceptual, or physiological events, the system is thrown off balance with conflicting signals to and from the brain at a reflex level, leading to stuttering. * Various studies found slower reaction times for PWS for some tasks * Reich concluded that PWS had longer initiation times for speech vocalization * Most studies point to slower laryngeal, oral, and manual reaction times for stutterers * Webster found that PWS made more errors and were slower in their performance, and were more susceptible to interference when they were asked to perform a second manual motor task simultaneous with finger tapping. * Yairi found that preschool children near onset of stuttering had slower speaking rates * Kloth found that **children who stutter (CWS)**' speech near the stuttering onset, contained imperceptible speech aberrations such as faster speaking rate * Ambrose: Perhaps young children who stutter, as a group, do not exhibit pervasive deficits in speech motor function, but instead may exhibit different thresholds for perturbation. * Forster and Webster tested the function of the supplementary motor area (SMA) using a finger-tapping task and a bimanual crank turning task. The recovered group (individuals who have recovered from stuttering) performed similarly to the control group (i.e., non-stutterers), but the persistent group had poorer skills. They concluded that the SMAs of the persistent individuals continued to function less than optimally. * Fox found overactivation in the right hemisphere of PWS during speaking, notably in the SMA, premotor areas, and cerebellum. However, when PWS read in chorus and were fluent, many of the differences in their brain activation patterns were reduced or even disappeared. * Ingham found activation abnormalities in motor planning brain areas **Genetics** * Various investigations explored stuttering in twins * Ambrose focused on separate segregation analyses for the families of children who recovered from stuttering (excluding persistent stuttering relatives) and the families of children who persisted in stuttering (excluding recovered stuttering relatives). Conclusions yielded the single highest likelihood for the presence of a major genecomponent (SML) in addition to MFP contributions. Indicating that the SML component involves one major gene that is present in both forms of stuttering: persistent and recovered. But, for the MFP parameters, the heritability component (phenotypic variation attributed to apolygenic, additive effect) differed. They concluded that CWS and family with persistent stuttering would tend to follow the same pattern. And vice versa, children who stutter but have a familial tendency of recovered stuttering would tend to follow that pattern. * It's important to remember that the division of stuttering into persistent and recovered subtypes could be a false dichotomy, and that there might be a better way to classify types of stuttering. **Conclusion** * If stuttering was completely governed by genetics, then if one identical twin stuttered, his or her twin would also stutter, and that is not the case—the rate is considerably less than 100, revealing the existence of strong environmental factors * Starkweather & Gottwald's Demands and Capacities model states that when demands exceed capacities, breakdown (stuttering) occurs, whereas Ratner’s trade-off hypothesis is based on uneven resource allocation, so that if resources are diverted for a challenging task, other functions may suffer. * We are not yet at a point to propose an encompassing detailed model of the cause of stuttering. * We do not yet know what such genes actually do, how they interact with each other, or how they interact with the environment. * The best bet may be that there is a deficit in the left hemisphere affecting both auditory and motor functions, and that the right hemisphere perhaps attempts to compensate, and one or more parts (subsystems) of the complex multilevel sensory and motor system responsible for the planning and orderly execution of fluent speech are fragile and easily perturbed. * In persistent stuttering, the left hemisphere system may be wired differently and less efficiently, but may attempt to developcoping strategies, compensating with the right hemisphere. * Those who stutter mildly and/or occasionally have successfully developed organized wiring mechanisms to circumvent the problem areas. Those who stutter consistently or severely manage to use available pathways but cannot maintain or develop consistent new efficient wiring. * The neural system of a child who fully and naturally recovers from stuttering may develop unevenly but become indistinguishable from that of a child who is normally fluent. * Travis' cerebral dominance theory states that stuttering “reflects a certain lack of maturation of the central nervous system which either does not afford integration of the highest neurophysiologic levels involved in speech or predisposes these levels to disintegration by various types of exogenous or endogenous stimuli”. This is very similar to the current position on the etiology of stuttering—but now we are accumulating concrete evidence to support it In conclusion, we need to ask the primary questions: 1. What is stuttering a symptom OF? 2. What are we trying to explain? 3. Where, in the fluency-generating system, does the breakdown - stuttering - occur? 4. Do breakdowns occur at multiple sites? 5. Is it components or connections that are aberrant? 6. What are the types of genes that could cause the types of effects in the brain that could cause the types of aberrant brain activity that could cause the types of stuttering symptoms? 7. How do we go from genes and nonshared environmental factors to a fragile fluency-generating system that is susceptible to breakdowns related to/from factors in the spheres of linguistic complexity, time pressure, excitement or anxiety, and other specifics susceptible to interference? 8. Does the most primal deficit lie in auditory processing, or central processing, or speech planning? 9. What are the subtypes of stuttering in specifics? 10. This mechanism must also explain how so many children stutter even severely and yet recover completely without formal intervention, whereas others stutter lifelong in spite of treatment